scholarly journals Intracellular Low Iron Exerts Anti-BK Polyomavirus Effect by Inhibiting the Protein Synthesis of Exogenous Genes

Author(s):  
Jiajia Sun ◽  
Yejing Shi ◽  
Huichun Shi ◽  
Yumin Hou ◽  
Chunlan Hu ◽  
...  

BKPyV poses a serious threat to the health of immunocompromised patients, and there are currently no curative drugs. Understanding the relationship between the virus and intracellular environment contributes to the discovery of antiviral targets.

Cancers ◽  
2021 ◽  
Vol 13 (22) ◽  
pp. 5867
Author(s):  
Mara Klöhn ◽  
Jil Alexandra Schrader ◽  
Yannick Brüggemann ◽  
Daniel Todt ◽  
Eike Steinmann

Hepatitis E virus infections are the leading cause of viral hepatitis in humans, contributing to an estimated 3.3 million symptomatic cases and almost 44,000 deaths annually. Recently, HEV infections have been found to result in chronic liver infection and cirrhosis in severely immunocompromised patients, suggesting the possibility of HEV-induced hepatocarcinogenesis. While HEV-associated formation of HCC has rarely been reported, the expansion of HEV’s clinical spectrum and the increasing evidence of chronic HEV infections raise questions about the connection between HEV and HCC. The present review summarizes current clinical evidence of the relationship between HEV and HCC and discusses mechanisms of virus-induced HCC development with regard to HEV pathogenesis. We further elucidate why the development of HEV-induced hepatocellular carcinoma has so rarely been observed and provide an outlook on possible experimental set-ups to study the relationship between HEV and HCC formation.


1976 ◽  
Vol 20 (1) ◽  
pp. 207-213
Author(s):  
F. Giannelli ◽  
S.A. Pawsey

Patients with Xeroderma pigmentosum and defective DNA excision repair can be distinguished as a rapid (r-XP) and slow (s-XP) complementing variety. When fused with normal cells, fibroblasts from the r-XP are complemented rapidly and in the absence of protein synthesis while those from the s-XP are complemented slowly by a process partly, but not entirely, dependent on protein synthesis. Heterokaryons with different ratios of r-XP to s-XP nuclei (i.e. 1:1-5 and 1-5:1) and control heterokaryons containing one normal and 1-5 r- or s-XP nuclei show that if cell fusion and incubation is conducted in medium preventing protein synthesis, the rXP cells do not complement the s-XP partner at all and, conversely, that the latter is not as effective as normal cells at complementing the rXP partner. On the contrary, if protein synthesis is permitted, the 2 types of XP cells complement each other in a gene dose-dependent manner and to an extent similar to that observed in the control heterokaryons. These findings indicate that the r- and s-XP varieties are caused by mutations at different loci and suggest that the products of these loci interact to produce a functional unit which is present in normal control cells but absent in the XP strains. The relationship between the complementation groups described here and those already reported in the literature being investigated.


PLoS ONE ◽  
2012 ◽  
Vol 7 (12) ◽  
pp. e51890 ◽  
Author(s):  
Gaetano Invernizzi ◽  
Francesco A. Aprile ◽  
Antonino Natalello ◽  
Andrea Ghisleni ◽  
Amanda Penco ◽  
...  

Weed Science ◽  
1986 ◽  
Vol 34 (3) ◽  
pp. 373-376 ◽  
Author(s):  
Cynthia Davis ◽  
Dean L. Linscott

Translocation and metabolism of14C-2,4-D [(2,4-dichlorophenoxy)acetic acid] and effects of 2,4-D on protein synthesis were compared in ‘T–68’ (2,4-D tolerant) and ‘Viking’ (susceptible) birdsfoot trefoil (Lotus corniculatusL.) in an attempt to elucidate some tolerance mechanisms. After14C-2,4-D was applied to upper trifoliate leaves, significantly less 2,4-D was found in stems, in leaves below the treated leaves, and in roots of T–68 compared to Viking. More 2,4-D was bound to alcohol-insoluble cellular constituents of T–68 leaves, stems, and roots. When alcohol-soluble components were fractionated, slightly more14C water-soluble compounds were found in T–68, indicating further inactivation by glycosylation. No amino acid-2,4-D conjugates were found. The rate of14CO2evolution from14C-2,4-D treated seedlings in T–68 was five times that in Viking. Protein synthesis appeared to be more rapid in T–68 but the relationship to 2,4-D was not clear. In part, 2,4-D resistance in T–68 may result from its ability to inactivate 2,4-D by differential binding and conjugation and by side chain breakdown as indicated by14CO2release.


2019 ◽  
Vol 81 (3) ◽  
pp. 202-209 ◽  
Author(s):  
Michael I. Dorrell ◽  
Jennifer E. Lineback

The central dogma of molecular biology is key to understanding the relationship between genotype and phenotype, although it remains a challenging concept to teach and learn. We describe an activity sequence that engages high school students directly in modeling the major processes of protein synthesis using the major components of translation. Students use a simple system of codes to generate paper chains, allowing them to learn why codons are three nucleotides in length, the purpose of start and stop codons, the importance of the promoter region, and how to use the genetic code. Furthermore, students actively derive solutions to the problems that cells face during translation, make connections between genotype and phenotype, and begin to recognize the results of mutations. This introductory activity can be used as an interactive means to support students as they learn the details of translation and molecular genetics.


1971 ◽  
Vol 134 (4) ◽  
pp. 935-946 ◽  
Author(s):  
Saimon Gordon ◽  
Zanvil Cohn

Dormant macrophage nuclei initiate DNA synthesis 2–3 hr after fusion of macrophages with exponentially growing melanoma cells. Cycloheximide treatment (1–5 µg/ml) of heterokaryons during the preceding lag period inhibits the initiation of macrophage DNA synthesis, in a reversible fashion. Each type of cell was also treated with streptovitacin A, an irreversible inhibitor of protein synthesis. Pretreatment of the melanoma cells (0.5–2 µg/ml), 1 hr before fusion, inhibited the induction of macrophage DNA synthesis in heterokaryons, whereas pretreatment of macrophages (1–20 µg/ml) had no effect. Melanoma cell pretreatment reduced the incorporation of leucine-3H into the cytoplasm and nuclei of heterokaryons, whereas macrophage pretreatment had no effect. These experiments suggested that melanoma proteins played an important role in the initiation of macrophage DNA synthesis. The relationship between the melanoma cell cycle and macrophage DNA synthesis was studied with synchronous melanoma cells. If the melanoma cells were in S phase at the time of fusion, macrophage DNA synthesis occurred 2 hr later. However, the fusion of melanoma cells in G1 delayed macrophage DNA synthesis until the melanoma nuclei had entered S. Experiments with actinomycin and cycloheximide showed that RNA and protein, essential to achieve DNA synthesis in the macrophage nucleus, were made during late G1 as well as S. Melanoma cells and macrophages differ in their radiolabeled acid-soluble products after incubation in thymidine-3H. Thymidine taken up by the macrophage remained unphosphorylated, whereas it was recovered mainly as thymidine triphosphate from melanoma cells. These findings, as well as those reported previously, suggest that the melanoma cell provides the RNA, protein, and precursors which initiate macrophage DNA synthesis. In the absence of a requirement for new macrophage RNA and protein synthesis, other changes must be responsible for the 2 hr delay in DNA synthesis. These may involve physical changes in DNA, associated with swelling, as well as the transport of melanoma products into the macrophage nucleus.


1976 ◽  
Vol 71 (2) ◽  
pp. 383-394 ◽  
Author(s):  
R L Hallberg ◽  
P J Bruns

Ribosome contents of growing and 12-h-starved Tetrahymena pyriformis (strain B) were compared. These studies indicate that (a) starved cells contain 74% of the ribosomes found in growing cells, (b) growing cells devote 20% of their protein synthetic activity to ribosomal protein production, and (c) less than 3% of the protein synthesized in starved cells is ribosomal protein. Ribosome metabolism was also studied in starved cells which had been refed. For the first 1.5 h after refeeding, there is no change in ribosome number per cell. Between 1.5 and 2 h, there is an abrupt increase in rate of ribosome accumulation but little change in rate of cell division. By 3.5 h, the number of ribosomes per cell has increased to that found in growing cells. At this time, the culture begins to grow exponentially at a normal rate. During the first 2 h after refeeding, cells devote 30-40% of their protein synthetic activity to ribosomal protein production. We estimate that the rate of ribosomal protein synthesis per cell increases at least 80-fold during the first 1-1.5 h after refeeding, reaching the level found in exponentially growing cells. This occurs before any detectable change in ribosome number per cell. The transit time for the incorporation of these newly synthesized proteins into ribosomes is from 1 to 2 h during early refeeding, whereas in exponentially growing cells it is less than 30 min. The relationship between ribosomal protein synthesis and ribosome accumulation is discussed.


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